Jarred Younger on CFS subgroups (video)

[silky]

Cellular exhaustion?

 

[Kati]

Cellular exhaustion?

Uhm, try this with a doctor and see how they react. The concept of cellular exhaustion is likely to land you in the psychiatrist office especially in certain countries. Medicine is not quite ready to hear this from patients.

 

[Ben H]

Thank you @Ben Howell for relaying Jared's response.

The problem I have is that what I got is not about fatigue. It is orthostatic intolerance, it is brain fog, it is post exertional 'malaise', it is lactic acid build-up if I over extend my capacity.

The concept of fatigue implies tiredness and the need to sleep, and by doing so one feels better. This is not the case with our illness. (at least mine). As I am typing, propped up in bed, my body is reminding me I should not be upright while thinking. This is not fatigue. This is gravity urging me to lay horizontal because the demand to my brain are too high. This is not fatigue.

I agree @Kati

The term 'fatigue' is not really representative at all of what I mean by it, and is traditionally thought as (cue stock CFS photo with student and head on desk).

To me it feels as if a plug has been pulled, and that plug was supplying me with energy. Literally a collapse and total absence of energy, which now persists 24/7. Like a switch has been flicked. (C'mon Ben, plug or switch, which is it!).

But to be honest while the name and the symptom names are incredibly important, I am waiting for the research to better classify/explain them based on the molecular mechanism(s) at play.

Just my 2c.


B

 

[boolybooly]

Thanks to Dr Jarred Younger.

He is absolutely right that identifying subgroups is the key to further research. If you are comparing results from 3 evenly divided subgroups with different causes all lumped together with CFS diagnosis then you will never get meaningful results.

Distinguishing the subgroups is an essential first step and this looks like a practical approach for getting around the obscuring issue of fluctuation (which IMHO hampered Kerr's and Gow's affymetrix studies) and turning it into data. I do hope it pans out as something useful.

 

[Anne]

Apologies if this has already been discussed, I haven't read the entire thread and i haven't watched the video (very tiny "computer envelope").

Cort writes that the CRP group is probably an infection group, because CRP is usually triggered by infection and not by autoimmune diseases. I would perhaps question that, seeing as CRP is a marker in several autoimmune rheumatological diseases elevated CRP.

In Rheumatoid Arthritis, for example, elevated CRP is one of the main markers. https://medlineplus.gov/rheumatoidarthritis.html#cat_92

Same with Polymyalgia Rheumatica https://medlineplus.gov/polymyalgiarheumatica.html#cat_92

and others.

Judging by this, I’m not sure the CRP group would necessarily be an infection group?

Does Younger connect CRP with infection and not with autoimmune diseases?

@mango FYI

A friend of mine emailed Jarred Younger to ask about this. He kindly replied (and quick!)

From Jarred Younger:
Yes – CRP is elevated in several autoimmune/rheumatic disorders as well as during infections. It is a very general test for inflammation.


It is true that if we just found elevated CRP in ME/CFS, that would not tell us much because many autoimmune disorders also involve significant fatigue. However, there are two unique elements to the CRP results we obtained. First, the CRP levels we saw actually weren’t elevated – they were below what most doctors would consider to be concerning (the average was around 3 mg/L). So, these individuals didn’t have CRP values that we would expect to see in classic autoimmune disorders. Also, it means that even low levels of CRP may be important in driving fatigue. Many tests have a floor cutoff at 10 mg/L, which wouldn’t even detect what we saw! The second unique element is that the day-to-day fluctuations were the most interesting part of CRP, not the average level. The question is why would CRP vary from day to day. Something underlying the CRP must be changing from day to day. I think bacteria and viri are good candidates because they are in a constant struggle with the immune system. But there are certainly other things that could drive changes in CRP. We don’t know, but the next step will be to test some possibilities using assays for viruses, bacteria, and other causes. The bottom line is that these results are very preliminary and we will definitely have to do other experiments to see what is happening.

Jarred

@mango @Johannawj @Lindberg